Establishment and characterization of epithelial and fibroblast cell lines from the bovine endometrium

Berg, Malia D.; Chen, Ziting; Dean, Matthew

doi:10.1007/s11626-021-00640-z

Cited by 2 publications

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Obesity is associated with lower fertility in women receiving donated ova or serving as surrogates ( DeUgarte et al 2010 , Bellver et al 2013 ). Type 2 diabetes and obesity are associated with hyperinsulinemia, hyperglycemia, and other systemic changes in metabolism, any of which could contribute to uterine dysfunction ( Lathi et al 2005 , Khaliq et al 2020 , Berg et al 2022 ). In mice, diet-induced obesity dysregulates glycolysis in the endometrium, impairs decidualization, and reduces litter size ( Chen et al 2023 ).…”

Section: Maternal Metabolism and Fertilitymentioning

confidence: 99%

“…In agreement, estradiol stimulates the production of IGF1 in the uterine stroma, and a study showed that IGF1 increases glycogen levels in BUTE cells ( Cooke et al 1997 , Gonzalez et al 2022 ). Insulin has also been shown to increase glycogen levels in uterine epithelial cells ( Dean and Rose 2018 , Berg et al 2022 ). This might indicate that hyperinsulinemia increases uterine epithelial glycogen storage.…”

Section: Metabolism and Secretion Of Nutrients By The Uterine Epitheliummentioning

confidence: 99%

See 1 more Smart Citation

Endometrial glucose metabolism during early pregnancy

Chen,

Dean

2023

Reproduction and Fertility

View full text Add to dashboard Cite

Approximately 50% of human pregnancies humans fail, most before or during implantation. One factor contributing to pregnancy loss is abnormal glucose metabolism in the endometrium. Glucose contributes to preimplantation embryo development, uterine receptivity, and attachment of the embryo. Across multiple species, the epithelium stores glucose as the macromolecule glycogen at estrus. This reserve is mobilized during the preimplantation period. Glucose from circulation or glycogenolysis can be secreted into the uterine lumen for use by the embryo or metabolized via glycolysis, producing ATP for the cell. The resulting pyruvate could be converted to lactate, another important nutrient for the embryo. Fructose is an important nutrient for early embryos, and the epithelium and placenta can convert glucose to fructose via the polyol pathway. The epithelium also uses glucose to glycosylate proteins, which regulates embryo attachment. In some species, decidualization of the stroma is critical to successful implantation. Formation of the decidua requires increased glucose metabolism via the pentose phosphate pathway and glycolysis. After decidualization, the cells switch to aerobic glycolysis to produce ATP. Paradoxically, the decidua also stores large amounts of glucose as glycogen. Too little glucose or an inability to take up glucose impairs embryo development and decidualization. Conversely, too much glucose inhibits these same processes. This likely contributes to the reduced pregnancy rates associated with conditions like obesity and diabetes. Collectively, precise control of glucose metabolism is important for several endometrial processes required to establish a successful pregnancy. The factors regulating these metabolic processes remain poorly understood.

show abstract

Section: Maternal Metabolism and Fertilitymentioning

confidence: 99%

Section: Metabolism and Secretion Of Nutrients By The Uterine Epitheliummentioning

confidence: 99%

Endometrial glucose metabolism during early pregnancy

Chen,

Dean

2023

Reproduction and Fertility

View full text Add to dashboard Cite

show abstract

Effect of estradiol and IGF1 on glycogen synthesis in bovine uterine epithelial cells

et al. 2022

View full text Add to dashboard Cite

Glycogen storage in the uterine epithelium peaks near estrus and is a potential source of glucose for the endometrium and embryos. However, the hormonal regulation of glycogen synthesis in the uterine epithelium is poorly understood. Our objective was to evaluate the effect of estradiol (E2) and insulin-like growth factor 1 (IGF1) on glycogenesis in immortalized bovine uterine epithelial (BUTE) cells. Treatment of BUTE cells with E2 (0.1-10 nM) did not increase glycogen levels. However, treatment of BUTE cells with IGF1 (50 or 100 ng/ml) resulted in a >2-fold increase in glycogen. To determine if the uterine stroma produced IGF1 in response to E2, bovine uterine fibroblasts (BFIBs) were treated with E2, which increased IGF1 levels. Immunohistochemistry showed higher levels of IGF1 in the stroma on day 1 than day 11, which coincides with higher glycogen levels in the uterine epithelium. Western blots revealed that IGF1 treatment increased levels of phospho-AKT, phospho-GSKβ, hexokinase 1, and glycogen synthase in BUTE cells. Metabolomic (GC-MS) analysis showed that IGF1 increased 3-phosphoglycerate and lactate, potentially indicative of increased flux through glycolysis. We also found higher levels of N-acetyl-glucosamine and protein glycosylation after IGF1 treatment, indicating increased hexosamine biosynthetic pathway activity. In conclusion, IGF1 is produced by uterine fibroblasts due to E2, and IGF1 increases glucose metabolism and glycogenesis in uterine epithelial cells. Glycogen stored in the uterine epithelium due to E2/IGF1 signaling at estrus could provide glucose to the endometrium or be secreted into the uterine lumen as a component of histotroph.

show abstract

Establishment and characterization of epithelial and fibroblast cell lines from the bovine endometrium

Cited by 2 publications

References 19 publications

Endometrial glucose metabolism during early pregnancy

Endometrial glucose metabolism during early pregnancy

Effect of estradiol and IGF1 on glycogen synthesis in bovine uterine epithelial cells

Contact Info

Product

Resources

About